1. Field of the Invention
This invention relates generally to body-implantable, medical apparatus, and more particularly to a cardiac rhythm management device (CRMD) having a capability of recording polysomnogram (PSG) data and/or phonocardiogram (heart sound) data upon the detection of pre-programmed conditions or events.
2. Discussion of the Prior Art
State of the art implantable medical devices, such as pacemakers and defibrillators, typically embody a microprocessorbased controller capable of receiving as inputs, digitized signals corresponding to heart depolarization events and other sensor derived outputs and for controlling a pulse generator that generates tissue-stimulating pulses in accordance with a program stored in a memory for the microprocessor-based controller. Such devices also typically include a telemetry link whereby programmed data and operands can be exchanged between the implanted device and an external programmer/monitor.
The memory in the implant may also be used to record, when enabled, electrogram signals for later read-out and analysis by a medical professional.
It is also known that cardiac pacing can be used as a therapy for patients with congestive heart failure (CHF). Algorithms have been developed for establishing a AV-delay interval that optimizes the pumping performance of the sick heart.
In applying cardiac pacing as a treatment for CHF, not only is electrogram data derived from an implanted CRMD of interest, but other physiologic sensor derived data may also prove helpful in treating the patient. For example, heart sound data can prove meaningful.
As is well known, the first heart sound, S1, is initiated at the onset of ventricular systole and consists of a series of vibrations of mixed, unrelated, low frequencies. It is the loudest and longest of the heart sounds, has a decrescendo quality, and is heard best over the apical region of the heart. The tricuspid valve sounds are heard best in the fifth intercostal space, just to the left of the sternum, and the mitral sounds are heard best in the fifth intercostal space at the cardiac apex.
S1 is chiefly caused by oscillation of blood in the ventricular chambers and vibration of the chamber walls. The vibrations are engendered by the abrupt rise of ventricular pressure with acceleration of blood back toward the atria, and the sudden tension and recoil of the A-V valves and adjacent structures with deceleration of the blood by the closed A-V valves. The vibrations of the ventricles and the contained blood are transmitted through surrounding tissue and reach the chest wall where they may be heard or recorded.
In accordance with the present invention, an implanted CRMD may include an accelerometer as a sound transducer and because implanted in close proximity to the heart, may develop a robust electrical signal that can be digitized and stored in the memory of the implant.
The intensity of the first sound is primarily a function of the force of the ventricular contraction, but also of the interval between atrial and ventricular systoles. If the A-V valve leaflets are not closed prior to ventricular systole, greater velocity is imparted to the blood moving toward the atria by the time the A-V valves are snapped shut by the rising ventricular pressure, and stronger vibrations result from this abrupt deceleration of the blood by the closed A-V valves.
The second heart sound, S2, which occurs on closure of the semi-lunar valves, is composed of higher frequency vibrations, is of shorter duration and lower intensity, and has a more xe2x80x9csnappingxe2x80x9d quality than the first heart sound. The second sound is caused by abrupt closure of the semi-lunar valves, which initiates oscillations of the columns of blood and the tensed vessel walls by the stretch and recoil of the closed valve. Conditions that bring about a more rapid closure of the semi-lunar valve, such as increases in pulmonary artery or aorta pressure (e.g., pulmonary or systemic hypertension), will increase the intensity of the second heart sound. In the adult, the aortic valve sound is usually louder than the pulmonic, but in cases of pulmonary hypertension, the reverse is often true.
The third heart sound, which is more frequently heard in children with thin chest walls or in patients with left ventricular failure due to CHF, consists of a few low intensity, low-frequency vibrations. It occurs in early diastole and is believed to be due to vibrations of the ventricular walls caused by abrupt acceleration and deceleration of blood entering the ventricles on opening of the atrial ventricular valves.
A fourth or atrial sound, (S4), consisting of a few low-frequency oscillations, is occasionally heard in normal individuals. It is caused by oscillation of blood and cardiac chambers created by atrial contraction.
When S3 and S4 sounds are accentuated, it may be indicative of certain abnormal conditions and are of diagnostic significance. Therefore, the ability to store heart sound information for later playback can prove beneficial to medical professionals following patients in whom cardiac pacemakers and/or defibrillators are implanted.
In addition to heart sound information, benefit can also be derived from the storage and later read out from an implanted CRMD of respiratory related data. While external polysomnograph equipment can be worn for recording respiratory related data over extended time intervals, the ability to derive polysomnograms from an implanted CRMD can prove to be beneficial. Such things as Cheyne-Stokes respiration patterns, Biot""s respiration, Epnustic breathing and central neurogenic hypoventilation and hyperventilation can be detected and recorded.
In Cheyne-Stokes respiration, respiratory rate and tidal volume gradually increase, then gradually decrease to complete apnea, which may last several seconds. Then, tidal volume and breathing frequency gradually increases again, repeating the cycle. This pattern occurs when cardiac output is low, as in CHF, delaying the blood transit time between the lungs and the brain. In this instance, changes in respiratory center Pco2 lag changes in arterial Pco2. For example, when an increased Paco2 from the lungs reaches the respiratory neurons, ventilation is stimulated, which then lowers the atrial Pco2 level. By the time this reduced Paco2 reaches the medulla to inhibit ventilation, hyperventilation has been in progress for an inappropriately long time. When blood from the lung finally does reach the medullary centers, the low Paco2 greatly depresses ventilation to the point of apnea. Atrial Pco2 then rises, but a rise in respiratory center Pco2 is delayed because of low blood flow rate. The brain eventually does receive the high Paco2 signal, and the cycle is repeated. Cheyne-Stokes respiration also may be caused by brain injuries, in which respiratory centers correspond to changes Pco2 level are damaged.
It is accordingly a principal object of the present invention to provide an implantable CRMD capable of producing and storing in a memory phonocardiograms of heart sounds and polysomnograms reflecting respiratory events for later readout from the device via a conventional telemetry link used in such devices.
It is still another object of the present invention to establish certain triggering mechanisms for enabling the memory to capture certain respiratory patterns such as those related to Cheyne-Stokes patterns by monitoring tidal volume or respiratory rate variations with respect to a pre-determined threshold. Similarly, the system may be enabled to capture heart sound information when, for example, atrial fibrillation occurs or, perhaps, at a certain level of exercise.
The foregoing objects are achieved in accordance with the present invention by providing an implantable cardiac rhythm management device of a type having a microprocessor-based controller along with a memory. The CRMD may also comprise a pulse generator for producing cardiac stimulating pulses at times determined by the program run on the microprocessor-based controller. Alternatively, the implant may be a purely diagnostic device. The CRMD also incorporates a means for sensing at least one of respiratory related activity and heart sounds. A triggering device is incorporated that is responsive to a predetermined event for initiating storage of data pertaining to the sensed one of respiratory related activity and heart sounds in the memory. As an example, upon detection of a predetermined respiratory pattern, the memory may be enabled for storing polysomnogram data. Alternatively, the occurrence of an event, such as an onset of atrial fibrillation, may be used to trigger the memory so as to store phonocardiogram data. The recording function in the memory of the implanted device can also be manually triggered, using an external magnet.